The product of the retinoblastoma tumour suppressor gene, pRb, mediates control of the G1 to S phase transition by interacting with growth-regulating transcription factors, such as the E2F family [1, 2]. The Rb gene is frequently mutated in tumour cells, and can be inactivated through the physical association with viral oncoproteins such as adenovirus E1A [3]. Post-translational phosphorylation control of pRb by G1 cyclin-dependent kinases plays an important role in regulating pRb activity [4]. The p300/CBP transcriptional co-activator proteins are endowed with histone acetyltransferase (HAT), which is involved in regulating chromatin [6].